Cerebral White Matter

Abstract

Lesions of the cerebral white matter (WM) result in focal neurobehavioral syndromes, neuropsychiatric phenomena, and dementia. The cerebral WM contains fiber pathways that convey axons linking cerebral cortical areas with each other and with subcortical structures, facilitating the distributed neural circuits that subserve sensorimotor function, intellect, and emotion. Recent neuroanatomical investigations reveal that these neural circuits are topographically linked by five groupings of fiber tracts emanating from every neocortical area: (1) cortico-cortical association fibers; (2) corticostriatal fibers; (3) commissural fibers; and cortico-subcortical pathways to (4) thalamus and (5) pontocerebellar system, brain stem, and/or spinal cord. Lesions of association fibers prevent communication between cortical areas engaged in different domains of behavior. Lesions of subcortical structures or projection/striatal fibers disrupt the contribution of subcortical nodes to behavior. Disconnection syndromes thus result from lesions of the cerebral cortex, subcortical structures, and WM tracts that link the nodes that make up the distributed circuits. The nature and the severity of the clinical manifestations of WM lesions are determined, in large part, by the location of the pathology: discrete neurological and neuropsychiatric symptoms result from focal WM lesions, whereas cognitive impairment across multiple domains—WM dementia—occurs in the setting of diffuse WM disease. We present a detailed review of the conditions affecting WM that produce these neurobehavioral syndromes, and consider the pathophysiology, clinical effects, and broad significance of the effects of aging and vascular compromise on cerebral WM, in an attempt to help further the understanding, diagnosis, and treatment of these disorders.

Episodic memory and executive functions in cognitively healthy individuals display distinct neuroanatomical correlates which are differentially modulated by aging

“…Significant clusters included the superior longitudinal fasciculus (SLF), the anterior thalamic radiation (ATR), as well as the forceps minor and the dorsal aspect of corticospinal tract (Figure 3). For the SLF, the local maxima peaked around an area that corresponds to its second subdivision (SLF‐II), which connects the angular gyrus to the parieto‐occipital regions supporting visual awareness and maintenance of attention (Schmahmann, Smith, Eichler, & Filley, 2008). The ATR projects to medial prefrontal areas from the anterior thalamic nucleus, which in turn receives afferences from the hippocampus (Mamah et al, 2010).…”

Motor Recovery Mechanisms in Patients with Middle Cerebral Artery Infarct: A Mini-Review

“…The MCA territory is an important area for motor function because it is comprised of the CST, the corticoreticulospinal tract and neural tracts which are related with apraxia [4,5,6,7,8,9,10,11,12,13,14,15,16]. In addition, the MCA occupies the largest area among the cerebral artery territories and has many branches.…”

“…That seems to be related to the characteristics of the MCA territory for motor function. The MCA territory comprises the corticospinal tract (CST) which is mandatory for fine motor activity of hand, the corticoreticulospinal tract which is involved in postural control and locomotor function, the corticofugal fibers which are responsible for limb-kinetic apraxia, and the anterior portion of superior longitudinal fasciculus which is related with ideomotor apraxia [4,5,6,7,8,9,10,11,12,13,14,15,16]. …”

Association between Subcortical Lesions and Behavioral and Psychological Symptoms in Patients with Alzheimer's Disease

“…lacunes and WML, are overrepresented in patients with AD [16]. A causal relationship with cerebral amyloid angiopathy has been suggested [17], but more data indicates that most subcortical lesions are caused by small vessel disease [15,18,19]. The overrepresentation of the lesions in AD could be explained by the reserve capacity hypothesis, a mutual interaction or perhaps a common risk factor [20].…”